Gastric PgCO2 and Pg-aCO2 gap are related to D-lactate and not to L-lactate levels in patients with septic shock.

Abstract

Intestinal ischemia causes an increase in lactate production and gastric intramucosal carbon dioxide partial pressure (PgCO(2)). However, no linear relationship between systemic l-lactate levels and gastric tonometry during intestinal ischemia has been found, probably since l-lactate is rapidly cleared from the circulation by the liver. In contrast, the rate of d-lactate clearance from the circulation by the liver is considerably lower than that of l-lactate, and d-lactate may therefore be more closely related to measurements of gastric tonometry than l-lactate values. Prospective, observational study in a university-affiliated mixed intensive care unit. Twenty critically ill patients with septic shock. During the first 24 h of admission to the intensive care unit at least two blood samples were taken for d- and l-lactate measurements and arterial blood gases, Simultaneously, gastric PgCO(2) was measured using capnographic tonometry. The intramucosal-arterial PCO(2) gap was calculated using gastric intramucosal PgCO(2) and arterial PCO(2) from arterial blood. d-Lactate was significantly correlated to PgCO(2) values and to the mucosal-arterial PCO(2) gap. There was no relationship between l-lactate and PgCO(2) or the mucosal-arterial PCO(2) gap. d-lactate and l-lactate values were significantly correlated. During sepsis intestinal production of d-lactate is related to gastric intramucosal PCO(2). No such relationship was found between l-lactate values and PgCO(2)